Perioperative management of a case of peripartum cardiomyopathy for elective cesarean section
Shalendra Singh1, Nitesh Kumar1, George Cherian Ambooken1, Shibu Sasidharan1, Priya Taank2
1 Department of Anaesthesiology and Critical Care, Armed Forces Medical College, Pune, Maharashtra, India
2 Department of Ophthalmology, CH (SC), Pune, Maharashtra, India
Correspondence Address:
Dr. Shalendra Singh
Department of Anaesthesiology and Critical Care, Armed Forces Medical College, Pune - 411 040, Maharashtra
India
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/ijhas.IJHAS_283_20
Peripartum cardiomyopathy (PPCM) during pregnancy is relatively rare. The anesthesia management of any heart pathology during peripartum requires the most stringent and meticulous care at every step. We report a 27-year-old woman, a diagnosed case of PPCM with previous lower segment cesarean section (LSCS) admitted for elective LSCS
Keywords: Peripartum cardiomyopathy, Postpartum, Pregnancy
Heart failure during pregnancy is a relatively rare, albeit life-threatening complication of pregnancy. Peripartum cardiomyopathy (PPCM) is defined as a disease of unknown origin wherein left ventricular dysfunction occurs during late pregnancy or early puerperium.[1] The advent of echocardiography has facilitated better recognition and management of cases with cardiac dysfunction. The management of any heart-related pathology during pregnancy requires the most stringent and meticulous care at every step of management.[2] Here, we discuss the management of a patient with a history of PPCM during the subsequent delivery.
Case ReportA 27-year-old woman, a diagnosed case of PPCM with previous lower segment cesarean section (LSCS), was admitted for safe confinement of pregnancy and elective LSCS. She had a history of undergoing previous LSCS under subarachnoid block 4 years back, following which she developed breathlessness and palpitations in the postoperative period. Subsequently, she was managed conservatively as a case of acute respiratory distress syndrome in the intensive care unit (ICU). Evaluation revealed dilated left atrium/left ventricle (LA/LV) with severe LV dysfunction (ejection fraction [EF]: 34%), global hypokinesia, and mild mitral regurgitation.
Preanesthetic evaluation for present pregnancy revealed a thinly built woman (weight: 52 kg) with a pulse rate of 100 bpm, regular rhythm, normal volume, and blood pressure (BP) of 122/70 mmHg. On auscultation, S1 and S2 were heard, and no S3/S4 murmur was appreciated. She had no features of fluid overload. She was functionally staged as New York Heart Association-1 with no complaints of dyspnea on exertion, orthopnea, or paroxysm nocturnal dyspnea. Breath-holding time was 35 s. No pedal edema was noted, and jugular venous pressure was normal. Airway examination was essentially normal. Transthoracic two-dimensional echocardiography revealed an EF of 45% and fractional shortening (FS) of 22% with mild global hypokinesia and no pulmonary arterial hypertension. End-diastolic LV dimension was 54 mm. The diagnosis of PPCM with residual LV dysfunction was made, and a preliminary anesthetic plan of administering low-dose spinal anesthesia with invasive arterial BP and central venous pressure monitoring was made.
After applying the standard monitoring, the right radial artery and right internal jugular vein were cannulated for invasive hemodynamic monitoring. The patient was administered subarachnoid block in sitting position at L3–L4 intervertebral space with low dose of local anesthesia (LA) (1.0 ml of 0.5% hyperbaric bupivacaine). 20 mcg of fentanyl was used as additive to LA for postoperative analgesia. Co-loading with 500 ml of Ringer's lactate was done to avoid a fall in BP. Boluses as well as infusion of vasopressor drugs were kept loaded in addition to antiarrhythmic drugs and short-acting beta-blockers.
Five minutes after administering the block, the patient had an episode of tachyarrhythmia in the form of supraventricular tachycardia which was managed with small boluses of esmolol. A single live male baby was delivered with a vigorous cry immediately after birth. Pitocin 3 unit's slow intravenous (IV) bolus was given, followed by slow infusion dose started at rate of 3 units/h. Approximately 2–3 min after delivery of the baby, the patient developed hypotension (BP: 85/53 mmHg) which was promptly treated with multiple bolus doses of mephentermine (totaling 12 mg). Subsequent intraoperative course remained uneventful with normotension, stable hemodynamics, and adequate oxygenation. A total of 1000 ml of crystalloid was infused intraoperatively.
The patient was shifted to ICU for hemodynamic monitoring. Adequate and efficacious round-the-clock postoperative maintenance analgesia was initiated with IV paracetamol q 6 h, along with rescue opioid analgesics (fentanyl 50 mcg bolus). A restrictive fluid therapy was resorted to prevent fluid overload (with fluids limited to 2.5 L over 24 h). Postpartum low-dose ACE-inhibitor was initiated with sips of water on the 1st postoperative night. Prophylactic dose low-molecular-weight heparin was initiated 24 h postoperatively to prevent venous thromboembolism. A long-acting oral beta-blocker was added to cover for any tachyarrhythmia in the postpartum period. The patient was monitored for 3 days in ICU and later shifted to ward. She was discharged after 1 week of uneventful stay in the hospital.
DiscussionThe incidence of PPCM varies from 1 in 300 to 1 in 3000–4000 live births.[3] Risk factors include multiparity, African descent, maternal age >30 years, multiple pregnancy, tocolytic therapy, and hypertensive disorders in pregnancy.[4] The diagnostic criteria for PPCM include an onset of heart failure during last month of pregnancy to 5 months postpartum, with no other identifiable cause, and no known heart disease before pregnancy. Echocardiographic criteria include an LVEF <45%, FS <30%, and left ventricular end-diastolic dimension >27 mm/m2.[5] The distinguishing feature of PPCM as opposed to ischemic cardiomyopathy is the presence of global LV hypokinesia instead of a regional wall motion abnormality. Subsequent pregnancies carry a substantially high risk of mortality if the LV dysfunction persists. The goal of anesthetic management in a woman with suspected PPCM or a past history of PPCM in previous pregnancy aims at maintaining myocardial perfusion by avoiding hypotension, tachycardia, and arrhythmias, apart from optimizing cardiac output by maintaining preload, reducing afterload, and maintaining cardiac contractility. Neuraxial anesthesia achieves these goals by reducing afterload. It also avoids the use of cardiac depressant induction agents as well as volatile anesthetic agents used for general anesthesia. Neuraxial opioid aids inefficacious postoperative analgesia by negating the sympathetically mediated catecholamine surge-induced increases in systemic vascular resistance and hence afterload. Restrictive fluid strategy both intra/postoperatively in addition to the administration of angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers in the postpartum period is one of the important step during treatment. Beta-blockers may also be considered to prevent tachycardia in the postpartum period.
The main “take-away” lessons of this case report are that the combination of closed monitoring and maintaining myocardial perfusion by avoiding hypotension, tachycardia, and arrhythmias, apart from optimizing cardiac output by maintaining preload, reducing afterload, and maintaining cardiac contractility.
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The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
There are no conflicts of interest.
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